Chromosomal translocations play a vital role in the pathogenesis of many lymphomas.[1]
The t(14;18)(q32;q21) translocation is the most common chromosomal abnormality associated with Non Hodgkin Lymphoma.
It occurs in 85% of follicular lymphomas and 28% of higher-grade Non Hodgkin Lymphoma.[2]
This results in the juxtaposition of the bcl -2 apoptotic inhibitor oncogene at chromosome band 18q21 to the heavy chain region of the immunoglobulin (Ig) locus within chromosome band 14q32..
The t(11;14)(q13;q32) translocation has association with mantle cell lymphoma.[3]
It causes overexpression of bcl -1 (cyclin D1/PRAD 1), a cell-cycle regulator on chromosome band 11q13.[4]
The 8q24 translocations causes c-myc dysregulation.[5][6]
It is frequently seen in high-grade small noncleaved lymphomas such as Burkitt lymphoma, including the one associated with HIV infection.
The t(2;5)(p23;q35) translocation occurs between the nucleophosmin (NPM) gene and the anaplastic lymphoma kinase (ALK1) gene.[4][7]
This results in the expression of a fusion protein found in a majority of anaplastic large cell lymphomas.
Two chromosomal translocations, t(11;18)(q21;q21) and t(1;14)(p22;132), are associated with mucosa-associated lymphoid tissue (MALT) lymphomas.
The more common type such as t[11;18][q21;q21] translocates the apoptosis inhibitor AP12 gene with the MALT1 gene; resulting in the expression of an aberrant fusion protein.
The other translocation, t(1;14)(p22;132), involves the translocation of the bcl -10 gene to the immunoglobulin gene enhancer region.
Some viruses are involved in the pathogenesis of Non Hodgkin Lymphoma because of their ability to induce chronic antigenic stimulation and cytokine dysregulation resulting in uncontrolled B- or T-cell stimulation, proliferation, and lymphomagenesis.
Epstein-Barr virus (EBV) is a DNA virus that is associated with Burkitt lymphoma, lymphomas in immunocompromised patients; and sinonasal lymphoma.
Human T-cell leukemia virus type 1 (HTLV-1) causes a latent infection due to reverse transcription ability in activated T-helper cells.
It is endemic in certain areas of Japan and the Caribbean islands, and approximately 5% of carriers develop adult T-cell leukemia or lymphoma.
Hepatitis C virus (HCV) is associated with the development of clonal B-cell expansions, lymphoplasmacytic lymphoma; and Waldenström macroglobulinemia especially in the setting of essential mixed cryoglobulinemia.
Kaposi sarcoma–associated herpesvirus (KSHV) is associated with body cavity lymphomas in patients with immunocompromised state and in patients with multicentric Castleman disease.
Helicobacter pylori infection is associated with the development of gastrointestinal lymphomassuch as gastric mucosa-associated lymphoid tissue (MALT) lymphomas.